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  • At least genes are associated with familial LQTS


    At least 15 genes are associated with familial LQTS, with 3 of these genes accounting for 70–75% of cases [5]. Despite advances in the understanding of the molecular basis of LQTS, challenges remain in making the clinical diagnosis. Importantly, between 10–40% of gene carriers have normal QT intervals [9,10]. While molecular genetics has contributed to improvements in some aspects of diagnosis, due to the variability of the QT interval and variable penetrance and expressivity, there is still evidence of significant misdiagnosis and delay in diagnosis [11]. Studies cholesterol absorption inhibitor that describe the clinical and genetic features of LQTS have been mainly from Europe, North America, and Asia. To our knowledge, there are no reports of cohorts with LQTS from Australia. With a prevalence of 1:2000–3000 [12,13], LQTS is a rare but significant health problem, and thus, clinical and genetic data from a range of countries and ethnicities are important. This study sought to report the clinical and genetic features of a registry-based cohort of Australian cholesterol absorption inhibitor with LQTS.
    Materials and methods
    Conflict of interest
    Acknowledgments We thank all patients and families without whom this research would not be possible. JI is the recipient of a National Health and Medical Research Council (NHMRC) and National Heart Foundation of Australia Early Career Fellowship (#1036756). CS is the recipient of an NHMRC Practitioner Fellowship (#1059156). BG is the recipient of a National Heart Foundation Ph.D. Scholarship (#100294).
    Introduction For patients diagnosed with a prior myocardial infarction (MI), ventricular tachycardia (VT) is a life-threatening co-morbidity. Although implantable cardioverter defibrillators (ICDs) have been shown to reduce the risk of sudden death [1], they cannot by themselves, prevent the occurrence of arrhythmias. Recently, catheter ablation of ventricular tachycardia has been emerging as an effective therapy [2], but the optimal target and endpoint of the procedure are still controversial. The efficacy of radiofrequency catheter ablation (RFCA) for VT in the setting of a structural heart disease was commonly defined by arrhythmia inducibility with programmed electrical stimulation, at the end of the procedure. Abolition of late potential (LP) has recently been proposed to reduce the risk of VT recurrences and to provide a better follow-up outcome [3]. However, an extensive management of all abnormal local electrical activity within scar tissue requires prolonged procedure time and might lead to greater myocardial damage or adverse events.
    Material and methods
    Results During the initial electrophysiological study, at least one monomorphic VT was induced in 49 (96%) of the 51 patients. VT mapping was obtained in 27 patients (53%), while substrate mapping was obtained in 24 patients, because of hemodynamic stability or the non-inducibility of a sustained VT. Procedural success was obtained in 49 of the 51 patients (96%). Forty-two patients (82%) received an ICD implant after ablation and 35 patients (69%) were administered amiodarone. At the end of the procedure, all VTs were non-inducible in 30 patients, non-clinical hemodynamically unstable VT was inducible in 19 patients, and clinical VT was still inducible in 2 patients. According to the inducibility, the patients were divided into two groups(Figs. 1 and 2). The patient characteristics and electrophysiological data are listed in Tables 1 and 2. There were no significant differences between the two groups regarding age, gender, location of infarction, history of ES, and LVEF (34.3% vs. 31.7%; P=0.34). The average number of induced VTs before the ablation was significantly larger in the induced group (1.8±1.2 vs. 2.9±1.9; P=0.02). The procedure time and the number of RF applications were also significantly larger in the induced group. The identification of the channel during VT mapping was more likely in the non-inducible result group (50% vs. 19%; P=0.04). The location and electrogram amplitude of the critical channel is shown in Table 3. Majority of the critical channels were located in the scar area, with a signal amplitude <0.5mV on electrogram. No mitral isthmus VT was found in this study.